Metabolic Syndrome (MetS) is a constellation of deleterious cardiometabolic health conditions (e.g., diabetes, hypertension) that have been linked to cognitive impairment and accelerated cognitive decline in older adults. Research has shown that Latinos are at increased risk for developing MetS relative to non-Latino Whites and the prevention, maintenance, and treatment of cardiometabolic risk factors are largely contingent upon health insurance status. Within the United States there are considerable state-based differences in eligibility and access to health insurance coverage. Although Texas has the second largest population of Latinos, they are one of the most underinsured groups within the state. There is some evidence to suggest that inconsistent healthcare is associated with cognitive impairment among underserved/underprivileged groups. The current study sought to examine whether insurance status moderates the association between MetS and cognitive functioning in an effort to inform public health policy initiatives vital to reducing age-related health disparities amongst Latino older adults residing in Texas.

The study sample included 850 primarily Spanish-speaking (67.6%) Latino older adults (mean age = 63.1±7.81) largely of Mexican origin/descent (95%) enrolled in the Health and Aging Brain Study-Health Disparities. All participants completed neuropsychological testing, a health exam, and questions about health insurance coverage. MetS status (MetS+ vs. MetS-) was determined by abnormal clinical abdominal obesity, triglycerides, high-density lipoprotein, blood pressure, and fasting glucose values. Health insurance status was determined by current enrollment in any private or public insurance plan. Cognition was assessed with Digit Span, Logical Memory I and II, Trail Making Test (A and B), Spanish-English Verbal Learning Test, and Letter Fluency (FAS). Raw scores were converted to z-scores which were subsequently averaged into two distinct memory and executive functioning composite scores. ANCOVAs controlling for age, sex, education, APOE e4 positivity, annual income, and primary language status were used examine health insurance status x MetS interactions on cognitive composites.

Approximately 54.6% of the sample met clinical criteria for MetS+ and 23.6% endorsed having no health insurance. There were no significant group differences in the proportion of MetS+ and MetS- individuals with and without health insurance (X 2 = .002, p =.96). Results revealed there was a significant MetS x health insurance status interaction on the memory composite (F = 5.39, p = .02). Post-hoc comparisons revealed that Latino older adults without health insurance demonstrated poorer memory performance relative to those with health insurance in the MetS+ group (p=.02). In contrast, there were no significant differences in memory performance across insurance status in the MetS- group (p=.35). Finally, there was no significant MetS x health insurance interaction on executive functioning (p=.60).

Findings revealed that health insurance coverage differentially impacts memory, but not executive functioning, amongst Latinos with MetS+. Underinsured Latinos with chronic cardiometabolic health conditions may be at risk for poor memory outcomes and increasing access to affordable healthcare could help mitigate the adverse effects of MetS+ on memory. Future studies examining the relationship between health insurance, MetS status, and neuroimaging markers may yield additional insight into mechanisms underlying age-related dementia disparities.

Non-Hispanic Black older adults experience a disproportionate burden of Alzheimer’s Disease and related dementias (ADRD) risk compared to non-Hispanic White older adults. It is necessary to identify mechanisms that may be contributing to inequities in cognitive aging. Psychosocial stressors that disproportionately affect Black adults (e.g., discrimination) have the potential to impact brain health through stress pathways. The brain’s white matter, which appears to be particularly important for ADRD risk among Black older adults, may be uniquely vulnerable to stress-related physiological dysfunction. To further understand whether and how discrimination can affect ADRD risk, this study aimed to examine associations between multiple forms of racial discrimination and white matter integrity, operationalized through diffusion tensor imaging.

Cross-sectional data were obtained from 190 non-Hispanic Black residents aged 65+ without dementia in northern Manhattan. Racial discrimination was self-reported using the Everyday Discrimination and Major Experiences of Lifetime Discrimination scales. Example items from the Everyday Discrimination Scale include: “You are treated with less respect than other people”; “You are called names or insulted.” Example items from the Major Experiences of Lifetime Discrimination Scale include: “At any time in your life, have you ever been unfairly fired from a job?”; “Have you ever been unfairly denied a bank loan?” Racial discrimination was operationalized as experiences attributed to “race” or “skin color.” White matter integrity was assessed using fractional anisotropy (FA) via diffusion tensor imaging. Multivariable regression models evaluated the unique effects of everyday and major experiences of lifetime racial discrimination on mean FA in the whole brain and specific regions. Initial models controlled for age, sex/gender, intracranial volume, and white matter hyperintensities. Subsequent models additionally controlled for socioeconomic and health factors to consider potential confounders or mediators of the relationship between discrimination and white matter integrity.

Major experiences of lifetime discrimination were negatively associated with mean FA within the left cingulum cingulate gyrus and the right inferior fronto-occipital fasciculus. These associations persisted when controlling for additional covariates (i.e., education, depression, and cardiovascular diseases). In contrast, major experiences of lifetime discrimination were positively associated with mean FA within the right superior longitudinal fasciculus (temporal part). This association was attenuated when controlling for additional covariates. Everyday racial discrimination was not associated with mean FA in any regions.

These results extend prior work linking racial discrimination to brain health and provide evidence for both risk and resilience among Black older adults. Major experiences of lifetime racial discrimination, a proxy for institutional racism, may have a stronger effect on white matter integrity than everyday racial discrimination, a proxy for interpersonal racism. Educational opportunities and cardiovascular risk factors may represent mediators between racial discrimination and white matter integrity. White matter integrity within specific brain regions may be a mechanism through which racially patterned social stressors contribute to racial disparities in ADRD. Future research should characterize within-group heterogeneity in order to identify factors that promote resilience among Black older adults.

To describe cognitive impairment in out-of-hospital cardiac arrest (OHCA) survivors, with the hypothesis that OHCA survivors would perform significantly worse on neuropsychological tests of cognition than controls with acute myocardial infarction (MI). Another aim was to investigate the relationship between cognitive performance and the associated factors of emotional problems, fatigue, insomnia, and cardiovascular risk factors following OHCA.

This was a prospective case control sub-study of The Targeted Hypothermia versus Targeted Normothermia after Out-of-Hospital Cardiac Arrest (TTM2) trial. Eight of 61 TTM2-sites in Sweden, Denmark, and the United Kingdom included adults with OHCA of presumed cardiac or unknown cause. A matched non-arrest control group with acute MI was recruited. We administered an extensive neuropsychological assessment at approximately 7 months post-cardiac event, including a neuropsychological test battery and questionnaires on anxiety, depression, fatigue, and insomnia, and collected information on the cardiovascular risk factors hypertension and diabetes. Z-scores of individual tests were converted to neuropsychological composite scores per cognitive domain (verbal, visual/constructive, working memory, episodic memory, processing speed, executive functions). Between-group differences on the neuropsychological composite scores were investigated with linear regression. Associations between anxiety, depression, fatigue, insomnia, hypertension, diabetes, and the neuropsychological composite scores among OHCA survivors were calculated with Spearman’s rho.

Of 184 eligible OHCA survivors, 108 were included (mean age = 62, 88% male), with 92 MI controls enrolled (mean age = 64, 89% male). Amongst OHCA survivors, 29% performed z <-1 indicating at least borderline-mild impairment in >2 cognitive domains, and 14% performed z <-2 exhibiting major impairment in >1 cognitive domain. OHCA survivors performed significantly worse than MI controls in episodic memory (mean difference, MD = -0.37, 95% confidence intervals [-0.61, -0.12]), verbal (MD = -0.34 [-0.62, -0.07]), and visual/constructive functions (MD = -0.26 [-0.47, -0.04]) on linear regressions adjusted for educational attainment and sex. When additionally adjusting for anxiety, depression, fatigue, insomnia, hypertension, and diabetes, processing speed (MD = -0.41 [-0.74, -0.09]) and executive functions (MD = -0.69 [-1.13, -0.24]) were also worse following OHCA. Depressive symptoms were associated with worse executive functions (rs = -0.37, p <0.001) and worse processing speed (rs = -0.27, p = 0.01) post-OHCA. Anxiety symptoms (rs = -0.21, p = 0.01) and general fatigue (rs = -0.24, p = 0.01) were associated with worse executive functions. Diabetes was associated with worse processing speed (rs = -0.20, p = 0.03), visual/constructive (rs = -0.29, p <0.001) and executive functions (rs = -0.25, p = 0.02), while hypertension and insomnia were not significantly associated with neuropsychological test performance.

Cognitive impairment is generally mild following OHCA, but most pronounced in episodic memory, executive functions, and processing speed. OHCA survivors performed worse than MI controls. We suggest that a post-OHCA follow-up service should screen for cognitive impairment, emotional problems, and fatigue.

Autistic youth have impaired executive functioning (EF) and these challenges increase throughout adolescence. Deficits in EF have been associated with poor adult outcomes, decreased availability for learning, and linked to academic outcomes. Specifically, flexible problem solving is greatly reduced in autistic youth. We aim to investigate how flexibility contributes to learning in autistic youth and their typically developing peers.

Participants included 44 teens with (n=22) and without (n=22) ASD. All teens were 14-18 years old (ASD M = 15.77, SD = 1.05; TD M = 15.73, SD = .96) with FSIQ 3 70 (ASD M = 105.92, SD= 16.17; TD M = 107.93, SD = 10.14). Teens with ASD met DSM-5 criteria for autism supported by the SCQ and/or ADOS-2. All participants completed the California Verbal Learning Task (Child or Third Edition) over zoom. Parents reported on their child’s flexibility skills on the Flexibility Questionnaire (FQ) which encompasses 5 subscales: routines/rituals, transitions, special interests, social flexibility, and generativity. Independent samples t-tests examined group differences in performance on the CVLT, measured by the long delay recall and learning slope. Bivariate correlations examined the relationship between learning and flexibility in the autistic group. Linear regression was used to determine how flexibility contributes to learning above and beyond age, gender, and diagnosis.

Autistic youth had significantly lower scores on the CVLT long-delay recall (t = 2.311, p = .026) and the learning slope (t = 1.186, p = .038) than their typically developing peers. Special interests on the FQ were related to both performance on the first trial of the CVLT (r = -.482 p = .023) and the short delay cued recall (r = -.469 p = .028) in the autistic group. Fewer transition related problems were predictive of higher scores on the CVLT above and beyond age, gender, and diagnosis (R2 = .366, B = - .088, p = .030).

Learning was significantly lower in autistic teens compared to their typically developing peers. Additionally, autistic youth had a less steep learning slope than their typically developing peers. Autistic youth may focus on the first group of words only and don’t flexibly update their list to add new words as the trials go on. Autistic youth with more restricted interests have difficulty with the first trial due to the shifting required when starting a new unfamiliar task. Additionally, youth with a greater focus on their own interests had more difficulty on cued recall indicating that these youth may have had trouble shifting when prompted to use semantic categories. Fewer challenges with transitions were a significant predictor of learning above and beyond age, gender, and diagnosis. Previous research has shown large discrepancies between parent-report and laboratory-based tasks in autistic youth. This project highlights two unique measures of different modalities that show similarities in their ratings emphasizing their potential as good representations of overall skills. Future research should utilize a larger sample size to continue to examine the role of flexible problem solving in working memory and learning in autistic youth.

Compensatory strategy training has been identified as a useful mechanism to improve everyday cognitive function among older adults with Mild Cognitive Impairment (MCI). Despite this, few studies have looked at cognitive factors that support adherence and engagement in these programs, which are key to maximizing benefit. The present study aimed to evaluate the relationship between cognition, adherence, and engagement during a group-based compensatory strategy training for people with MCI. We hypothesized individuals with better memory and executive function performance would show better adherence and higher engagement scores in cognitive training classes.

Twenty-five participants enrolled in Emory University's Charles and Harriet Schaffer Cognitive Empowerment Program (CEP) completed an 11-week compensatory strategy training group (CEP-CT). CEP-CT is adapted from Ecologically Oriented Neurorehabilitation to be suitable for people with MCI. Participants enrolled were on average 74.3 years old (SD= 5.4), 52% Male, primarily Caucasian (80%; 16% African American), and college educated (M= 16.5 years; SD= 2.7). All participants received clinical diagnoses of MCI prior to enrollment in the program. Participants completed multiple cognitive measures, including Montreal Cognitive Assessment (MoCA), Hopkins Verbal Learning Test (HVLT), Trail Making Test A & B (TMT), Number Span Forward (NSF) and verbal fluency (S-words and Animals). For all group sessions, class attendance (present vs. not present) was recorded for each participant and their care partner, and engagement ratings for participants were recorded by the facilitator on a 1 to 5 scale (higher scores indicate better engagement). Outcomes include adherence to cognitive training (percentage of sessions attended; M= 82% class attendance, SD= 18%) as well as the average engagement ratings across 11 weeks (M= 3.25, SD= .40).

Bivariate Pearson correlations revealed that individuals who attended more classes also demonstrated better engagement in class, r= .44, p= .03. Class attendance was significantly related to performance on measures of memory and executive function (HVLT: r= -.42, p= .04; TMT-B: r= .69, p= .04), such that participants who performed worse on these measures attended more CEP-CT classes. Average engagement ratings were unrelated to cognitive performance.

Results did not support initial hypotheses, and instead indicate individuals with poorer performance on measures of memory and executive function had better adherence to CEP-CT classes, as measured by attendance. These results may indicate individuals experiencing cognitive difficulties are more likely to attend cognitive training classes. Subjective engagement ratings were unrelated to cognition; however, individuals who attended more sessions were more engaged in cognitive training classes. Future areas of research include objective measurement of class engagement as well as the incorporation of nuanced adherence metrics to further elucidate the relationship between these factors and cognition in MCI.

Despite associations between hypoglycemia and cognitive performance using cross-sectional and experimental methods (e.g., Insulin clamp studies), few studies have evaluated this relationship in a naturalistic setting. This pilot study utilizes an EMA study design in adults with T1D to examine the impact of hypoglycemia and hyperglycemia, measured using CGM, on cognitive performance, measured via ambulatory assessment.

Twenty adults with T1D (mean age 38.9 years, range 26-67; 55% female; 55% bachelor’s degree or higher; mean HbA1c = 8.3%, range 5.4% - 12.5%), were recruited from the Joslin Diabetes Center at SUNY Upstate Medical University. A blinded Dexcom G6 CGM was worn during everyday activities while completing 3-6 daily EMAs using personal smartphones. EMAs were delivered between 9 am and 9 pm, for 15 days. EMAs included 3 brief cognitive tests developed by testmybrain.org and validated for brief mobile administration (Gradual Onset CPT d-prime, Digit Symbol Matching median reaction time, Multiple Object Tracking percent accuracy) and self-reported momentary negative affect. Day-level average scores were calculated for the cognitive and negative affect measures. Hypoglycemia and hyperglycemia were defined as the percentage of time spent with a sensor glucose value <70 mg/dL or > 180 mg/dL, respectively. Daytime (8 am to 9 pm) and nighttime (9 pm to 8 am) glycemic excursions were calculated separately. Multilevel models estimated the between- and within-person association between the night prior to, or the same day, time spent in hypoglycemia or hyperglycemia and cognitive performance (each cognitive test was modeled separately). To evaluate the effect of between-person differences, person-level variables were calculated as the mean across the study and grand-mean centered. To evaluate the effect of within-person fluctuations, day-level variables were calculated as deviations from these person-level means.

Within-person fluctuations in nighttime hypoglycemia were associated with daytime processing speed. Specifically, participants who spent a higher percentage of time in hypoglycemia than their average percentage the night prior to assessment performed slower than their average performance on the processing speed test (Digit Symbol Matching median reaction time, b = 94.16, p = 0.042), while same day variation in hypoglycemia was not associated with variation in Digit Symbol Matching performance. This association remained significant (b = 97.46, p = 0.037) after controlling for within-person and between-person effects of negative affect. There were no significant within-person associations between time spent in hyperglycemia and Digit Symbol Matching, nor day/night hypoglycemia or hyperglycemia and Gradual Onset CPT or Multiple Object Tracking.

Our findings from this EMA study suggest that when individuals with T1D experience more time in hypoglycemia at night (compared to their average), they have slower processing speed the following day, while same day hypoglycemia and hyperglycemia does not similarly impact processing speed performance. These results showcase the power of intensive longitudinal designs using ambulatory cognitive assessment to uncover novel determinants of cognitive variation in real world settings that have direct clinical applications for optimizing cognitive performance. Future research with larger samples is needed to replicate these findings.

Older adults represent the fastest-growing population of individuals with epilepsy with an incidence that peaks after age 65. Patients with late-onset epilepsy (LOE) have a multitude of risk factors for accelerated cognitive and brain aging, including vascular and metabolic risk factors. Despite this, there are few studies investigating the cognitive profiles of older adults with LOE, a neglected area in aging research. We examine the cognitive profiles of older adults with LOE and determine the contribution of demographic and vascular risk factors to impairment.

Participants were part of the Atherosclerosis Risk in Communities Study (ARIC) and the incidence of epilepsy was identified using ARIC hospitalization records and Centers for Medicare and Medicaid Services claims data from 1991 to 2015. Approximately 1.8% of the participants with sufficient Medicare coverage data were classified as having LOE (LOE n=281; Non-LOE n=9808). Vascular, lifestyle, and cognitive data were obtained from the ARIC Neurocognitive Study (ARIC-NCS) which consisted of three visits since 2011. Participants with ARIC-NCS visits completed after the onset of seizures were included in the final sample. Non-LOE participants with normal cognition (Black: n=603 and White: n=2543 participants independently) were used to generate z-scores across tests of language, memory, executive function, and processing speed/attention. Impairment was defined as <1.5 standard deviations below the mean of the normative sample. Stepwise regressions were conducted to examine the contribution of demographic (age, race, sex, education) and vascular risk factors (hypertension, diabetes, hyperlipidemia, obesity, smoking) to cognitive performance.

Average age of first seizure of all LOE participants (n=281) was 76.23 (SD=6.24), 55.9% female, 30.7% Black/African American, and the majority had either a college (28.1%) or high school degree (26%). Fifty-six LOE participants had ARIC-NCS visits after the onset of seizures (average age=79.84, SD=5.17, 57.1% female, 32.1% Black). Approximately 67.9% of the sample had at least one vascular risk factor with 81.5% having hypertension, 37% diabetes, 26.4% hyperlipidemia, 20.4% obesity (BMI>30), and 4.5% current smoker. The most frequently impaired domains were language (naming=29.7%; animal fluency=20%; letter fluency=30%) and memory (prose immediate recall=18.4%; prose delayed recall=44.7%; word delayed recall=19.4%). Higher education was associated with better naming (b=0.801, p=0.040). Female sex (b=-0.799, p=0.017) and lower education levels (b=0.418, p=0.050) were associated with poorer immediate prose recall. Older age was associated with poorer delayed prose recall (b=-0.191, p=0.036). Hypertension was associated with worse digit span backward (b=-0.942, p=0.002).

In older adults with LOE, language and memory were the most commonly impaired cognitive domains, similar to studies in early onset epilepsy. Vascular risk factors were prevalent among LOE and hypertension was associated with worse working memory. Further, important demographic factors (sex, education, and age) were associated with the extent of cognitive impairment. Characterizing cognitive profiles in LOE and determining the contribution of demographic and vascular factors to impairment could help to identify patients at risk for future cognitive decline and/or the development of LOE itself, as well as interventions aimed at reducing the risk of further decline.

Quantitative Susceptibility Mapping (QSM) is an MRI-based technique that sensitively measures in-vivo iron deposition via relaxation and magnetic susceptibility of brain tissue. Iron is essential for brain homeostasis, including oxidative metabolism, formation and maintenance of neural networks, and myelin synthesis. While increased levels of iron deposition occur during normal aging, high levels may have detrimental effects. Previous work has linked excessive brain iron accumulation to oxidative stress, beta-amyloid and tau toxicity, neurodegeneration, and cognitive dysfunction, particularly memory loss. Physical activity, on the other hand, correlates with higher synaptic integrity and memory performance, even in the presence of neuropathology. To date, it is unknown how physical activity may affect iron deposition-related cognition changes. We examined the moderating role of physical activity on the relationship between QSM hippocampal iron deposition and verbal memory in typically aging adults.

62 cognitively unimpaired older adults from the UCSF Memory and Aging Center (age mean(SD) = 78.34(7.28) years; 56% women; education mean(SD) = 17.94(1.72) years; 85% non-Hispanic White) completed neuropsychological testing and brain MRI during annual research visits, followed by Fitbit™ physical activity monitoring for 30 days. Average total daily steps were aggregated. Participants completed 3T Prisma neuroimaging with QSM, and regional iron deposition levels were quantified. All subjects also underwent diffusion tensor imaging (fractional anisotropy). Verbal memory was assessed via long delay free recall scores from the California Verbal Learning Test II (CVLT-II). Linear regression examined verbal memory as a function of hippocampal QSM (bilateral), physical activity, and their interaction. Models covaried for age, sex, and education. Additional models separately examined left and right hippocampal QSM, as well as subcortical QSM to determine lateralization and specificity of verbal memory effects to hippocampal iron deposition, respectively.

Univariably, higher bilateral hippocampal QSM correlated with worse verbal memory (r= 0.35; p= 0.015). Adjusting for demographics, physical activity moderated the relationship between bilateral hippocampal QSM and verbal memory (ß= 0.41, p= 0.011), such that at higher levels of physical activity, the negative relationship between hippocampal QSM and verbal memory was significantly attenuated. Results persisted when adjusting for DTI integrity of the uncinate fasciculus and fornix white matter tracts. Lateralization models were both significant, suggesting that results were not dominantly driven by either left (ß= 0.34, p= 0.048), or right (ß=0.31, p= 0.035) hippocampal QSM. In contrast, subcortical QSM did not correlate with memory performance (r= 0.13, p > 0.05) or interact with physical activity on verbal memory outcomes (p > 0.05).

Physical activity significantly moderated the negative relationship between hippocampal QSM and verbal memory performance. Higher exercise engagement may buffer the adverse effect of hippocampal iron deposition on memory, potentially through its role in maintenance of myelin and synaptic integrity and/or protecting against other neurotoxic events (e.g., oxidative stress, neuronal cell death). Our results support that physical activity continues to be a modifiable risk factor that may offer a protective role in neurobiological pathways of memory and cognitive decline.

In recent years, rates of alcohol consumption and alcohol use disorder have steadily increased among adults age 60 and older. Large studies have demonstrated that moderate-to-heavy alcohol consumption (>7 drinks per week) is a risk factor for developing various types of dementias. The effects of alcohol-related problems on cognition are less clear, and are particularly understudied in older adults. Similarly, while there is an established link between worse cognition and financial exploitation vulnerability in older adults, no studies have examined relationships between alcohol-related problems and financial exploitation in this population. The current study therefore explores whether alcohol-related problems are associated with neuropsychological performance and financial exploitation vulnerability in a sample of older adults.

Participants were a community sample of cognitively unimpaired adults over the age of 50 (N = 55, Age M(SD) = 69.1(6.2), 74.5% female, Years of education M(SD) = 16.8(2.3)). Interested individuals were excluded if they reported current or past substance use disorders. Participants completed a laboratory visit that included a neuropsychological assessment. Measures included the NIH Cognition toolbox, CVLT-II, Digit Span, Trails A/B, Benson Complex Figure Recall, and Verbal Fluency: Phonemic and Semantic, from the Alzheimer’s Disease Centers’ Uniform Data Set (UDS) version 3. Participants completed the CAGE Alcohol Abuse Screening Tool and the Short Michigan Alcohol Screener Test - Geriatric Version (SMAST) to assess alcohol-related problems. Both measures are used as clinical screening tools to measure likelihood of a substance use disorder and produce a summary score (0-4 for CAGE, 010 for SMAST) tabulating symptoms of alcohol-related problems. Participants also completed the Perceived Financial Vulnerability Scale (PFVS) to assess financial exploitation vulnerability. As a significant number of participants reported no drinking and therefore no alcohol-related problems, negative binomial regressions were used to test associations between neuropsychological measures, financial exploitation vulnerability, and alcohol-related problems.

After covarying for age and sex, SMAST was negatively associated with NIH toolbox total cognition (B(SE) = -.14(.07), p<.05) and marginally negatively associated with fluid cognition (B(SE) = -.07(.04), p=.06). Neither SMAST nor CAGE scores were significantly associated with performance on any other neuropsychological test (ps = .13-.99). SMAST was positively associated with financial exploitation vulnerability (B(SE) = .31(.16), p = .05); this effect remained significant after covarying for NIH total composite score in a secondary analysis.

In a community sample of cognitively unimpaired, low-drinking adults over the age of 50, more alcohol-related problems were associated with worse NIH toolbox cognition scores. Similarly, more alcohol-related problems were associated with greater financial exploitation vulnerability, and this relationship was not driven by worse cognition. These results suggest that even low amounts of drinking and alcohol-related problems may be associated with cognition and financial exploitation vulnerability in cognitively unimpaired older adults. This study also corroborates the use of the SMAST over the CAGE in older adult populations that may be more sensitive to cognitive changes.

This was a pilot study testing a cognitive enhancement program to improve rate of cognitive recovery in early substance abuse treatment. It is hypothesized that if patients were able to accelerate the rate of cognitive improvement, they may be able to better engage in substance abuse treatment and potentially have better long-term outcomes.

Participants were 47 adults newly admitted to a residential substance abuse treatment facility (74.5% male, 76.6% white, mean age=34.5 years, education=12+ years). All were post-detox. All were being treated for opioid abuse, with the majority in treatment for polysubstance abuse. Participants were randomly assigned to either the intervention group (BrainHQ research cognitive training program) or active control group (inert computer games) and completed 34 training sessions per week for a minimum of 3 weeks. NIH Toolbox cognition battery was administered at baseline and endpoint.

Regardless of study group, most participants had a significant improvement in cognitive performance across most subtests and composite scores of the NIH Toolbox cognition battery. The RAVLT and Oral Symbol Digit subtests had the greatest change (p<.001) for both groups, as well as a significant improvement (p=.002) in Cognitive Function Composite Score for both groups. The only difference between the control and intervention group was on the Pattern Comparison subtest, with the intervention group scoring significantly higher at endpoint (p=.004).

Although substance abuse is known to cause injury to the brain that may not be fully repaired by sobriety, cognitive recovery was significant in this group of patients during early inpatient treatment for opioid abuse. Although it has yielded significant effect in other patient populations, the BrainHQ program did not show a significant enhancement in cognitive recovery, compared to the active control group, in this pilot study of patients in treatment for opioid abuse. This study was limited by a small sample size and potential future variations should be considered, such as changes to intervention intensity and specific intervention exercises.

Early life adversity is strongly correlated with a number of negative health outcomes, with some of the highest risks are related to later illicit drug use and substance use disorders (SUDs). Specifically, it has been found that an ACEs score of >4 confers a 7-10-fold risk of substance abuse. Subsequent research has identified a number of neurobiological effects of childhood trauma, including structural and functional disruptions of the LHPA axis, the brain's primary stress-response system. It has been hypothesized that various trauma-induced neurobiological changes may lead to later physical health, mental health, and psychosocial problems in persons with early life adversity. One area that such changes might affect is a person's ability to stop abusing substances, with factors such as trauma-related mood, self-efficacy, or cognitive functioning as considerations in early treatment success. This study followed a group of participants in a residential substance abuse treatment program across their first month of abstinence, to assess natural change in cognitive performance as well as potential effect of early life adversity on changes in neuropsychiatric outcomes.

Participants were 37 adults (mean age=33.9 years, SD=6.7) who had completed detoxification and were first assessed during their first week of residential treatment. Follow-up assessment was completed 4 weeks later. Participants were primarily male (62%) and white (62%). They were all in treatment for opioid abuse, with a majority of participants reporting a history of polysubstance abuse. To measure adverse and protective factors, participants completed the Adverse Childhood Experiences scale and Protective And Compensatory Experiences Scale at baseline. Participants also completed the NIH Toolbox cognition battery and a set of self-report measures of cognitive functioning, mood, anxiety, and self-efficacy at baseline and follow up.

Results of paired samples t-test comparison between baseline and follow-up testing found a significant improvement in self-reported depression symptoms, anxiety symptoms, and self-efficacy (all p<.001). Interestingly, participants overall reported an increase in cognitive problems between baseline and retest, even though on objective cognitive testing (NIH Toolbox cognition battery) there was significant improvement in cognitive performance. Participants generally had a high level of childhood adversity (mean ACE score of 4.5), with an average level of childhood compensatory experiences. Considering the specific effect for childhood adversity, ACE score was found to be predictive in amount of anxiety and self-reported cognitive change but not for objective cognitive performance or change in other factors.

Consistent with previous research, these patients had a high level of past trauma, which interacted with a number of other neuropsychiatric measures and support the importance of assessing for trauma history and integrating trauma-focused treatment into substance abuse treatment programs.

Methamphetamine and cannabis are two widely used substances with possibly opposing effects on aspects of central nervous system functioning. Use of these substances is prevalent among people with HIV (PWH), though their combined effects on HIV-associated neurocognitive impairment (NCI) are unknown. Adverse effects of methamphetamine use on cognition are well documented. Cannabis may disturb cognition acutely, though its longer-term effects in PWH are not well understood. Our prior analysis of people without HIV (PWoH) found that cotemporaneous cannabis use was associated with better neurocognitive outcomes among methamphetamine users. The aim of this study was to assess how lifetime cannabis and methamphetamine use disorder relate to neurocognitive outcomes in PWH.

HIV-positive participants (n=472) were on average 45.6±11.5 years of age, male (86.4%), White (60.6%), and educated 13.9±2.5 years. Most participants were on ART (81.9%) and virally suppressed (70%). Participants were stratified by lifetime methamphetamine (M-/M+) and cannabis (C-/C+) DSM-IV abuse/dependence disorder into four groups: M-C- (n=187), M-C+ (n=68), M+C-, (n=82) and M+C+ (n=135) and completed a comprehensive neurobehavioral assessment. Demographically corrected T-scores and deficit scores were used for analyses. Group differences in global and domain NC performances (i.e., T-scores) were examined using multiple linear regression, holding constant covariates that were associated with study groups and/or cognition. Specifically, M+ participants displayed higher rates of Hepatitis C infection (p=.004), higher current depressive symptom scores (p<.001), and higher rates of detectable plasma HIV RNA (p=.014). Multiple logistic regression was used to test for group differences in probability of neurocognitive impairment (i.e., deficit scores>0.5), including the same covariates. Pooling data with a sample of HIV-negative participants (n=423), we used generalized linear mixed effect models to examine how neurocognitive performance and impairment profiles varied by methamphetamine and/or cannabis use group, HIV disease characteristics, and their interactions.

Compared to M+C+, M+C- performed worse on measures of executive functions (ß=-3.17), learning (ß=-3.95), memory (ß=-5.58), and working memory (ß=-4.05) and were more likely to be classified as impaired in the learning (OR=2.93), memory (OR=5.24), and working memory (OR=2.48) domains. M-C- performed better than M+C+ on measures of learning (ß=3.46) and memory (ß=5.19), but worse than M-C+ on measures of executive functions (ß=-3.90), learning (ß=-3.32), memory (ß=-3.38), and working memory (ß=-3.38). Generalized linear mixed effect models indicate that detectable plasma HIV RNA (ß=-1.85) and low nadir CD4 T-cell counts (nadir CD4<200; ß=-1.07) were associated with worse neurocognitive performance, and these effects did not differ in size or direction by substance use group.

In PWH, lifetime methamphetamine use disorder and both current and legacy markers of HIV disease severity are associated with worse neurocognitive outcomes. Cannabis use disorder does not appear to exacerbate methamphetamine-related deficits in PWH. Instead, results are consistent with findings from preclinical studies that cannabis use may protect against methamphetamine’s deleterious effects. Profile analysis models showed that participants with a history of cannabis use disorder display better overall neurocognitive performance than comparison (M-C-) participants. Mechanisms underlying a potential protective effect of cannabis may be elucidated by examining the temporal relationship between cannabis and methamphetamine consumption and neurocognitive performance.

Chronic alcohol consumption has been associated with widespread cognitive deficits, including psychomotor speed. Researchers have found impairments in reaction speed, information processing, and fine-finger movement in alcoholics (Oscar-Berman et al., 2015). There have also been mixed findings on the impact of duration of alcohol use on neurocognitive functioning (Beatty et al., 2000; Oscar-Berman et al., 2004). This meta-analytical study examines: (a) the performance of abstinent alcohol-dependent individuals on psychomotor speed using the Trail Making TestA (TMT-A), and (b) the effect of duration of alcohol use on TMT-A.

As part of a larger study, two researchers independently searched eight databases, extracted required data, and calculated effect sizes on neuropsychological data in alcohol dependent (AD) individuals. Inclusion criteria for articles were: (a) comparison of abstinent alcohol-dependent patients to healthy controls, (b) matched control group on age, education, or IQ, and (c) standardized neuropsychological testing. Exclusion criteria included: (a) diagnosis of Axis I disorders (other than alcohol dependence), (b) comorbidity with other disorders that impact neuropsychological functioning, or (c) not published or translated into English. Twenty-seven articles (AD n= 840 and HC n = 881) were analyzed in this study.

The TMT-A evidenced a statistically significant and medium effect size estimate (g = 0.624, p < 0.001). The heterogeneity of TMT-A was statistically significant (Q=61.935, df=26, p=0.000) and moderate (I2=58.021%). The meta-regression analysis between duration of alcohol use in days and TMT-A was not statistically significant (Q=0.012, df=1, p=0.913).

TMT-A detects psychomotor speed deficits associated with alcohol dependence. Duration of alcohol use did not affect TMT-A performance, suggesting that other factors may have moderated this relationship. Further research should analyze other factors that affect psychomotor performance in alcohol dependent individuals.

Verbal fluency consists of semantic and phonemic fluency and is often used to detect verbal ability and executive control (Shao et al., 2014). While research has found general verbal fluency impairments in chronic alcohol use, few studies have examined semantic and phonemic fluency separately (Stavro et al., 2012; Stephan et al., 2017). This meta-analytical study examines the performance of abstinent alcohol-dependent individuals on semantic fluency (categories) and phonemic fluency (letters).

As part of a larger study, two researchers independently searched eight databases, extracted required data, and calculated effect sizes on neuropsychological data in alcohol dependent (AD) individuals. Inclusion criteria for articles were: (a) comparison of abstinent alcohol-dependent patients to healthy controls, (b) matched control group on age, education, or IQ, and (c) standardized neuropsychological testing. Exclusion criteria included: (a) diagnosis of Axis I disorders (other than alcohol dependence), (b) comorbidity with other disorders that impact neuropsychological functioning, or (c) not published or translated into English. A total of 31 articles (AD n=1,080 and HC n=1,090) was analyzed in this study.

Semantic fluency evidenced a statistically significant and medium effect size estimate (g = 0.632, p < 0.001). The heterogeneity for semantic fluency was statistically significant (Q=152.468, df=20, p=0.000). Phonemic fluency evidenced a statistically significant and medium effect size estimate (g = 0.572, p < 0.001). The heterogeneity for phonemic fluency was also statistically significant (Q=236.697, df=24, p=0.000).

Deficits in semantic and phonemic fluency are both associated with alcohol dependence. Although some previous research has reported more frontal lobe impact of alcohol, which would be expected to impact phonemic more readily than semantic fluency, this is not evident in the current data. There are many possible reasons for this failure to observe this dissociation meta-analytically. Some potential reasons include the possibility that alcohol affects multiple regions of the brain, that both these measures are affected by alcohol but miss the subtlety associated with frontal damage, or the likelihood that when studies are aggregated in meta-analysis the heterogeneity results in a regression to the mean effect size. These and other reasons are not mutually exclusive and future research should attempt to examine these and other hypotheses.

Opioid use disorder (OUD) has been declared a national public health emergency leading to increased enrollment in medication assisted treatment (MAT) programs. Cognitive deficits are seen among those with OUD which can persist even with MAT. Moreover, cognitive deficits predict poor community and treatment outcomes. Neuropsychological evaluations can identify, diagnose, and provide treatment recommendations, and are associated with improved outcomes in non-substance use patient populations. Yet, patients with OUD rarely undergo neuropsychological assessment when participating in opioid use treatment. Teleneuropsychology (TNP) may increase access to care but has not been evaluated with people with substance use disorders (SUDs). This project used a mixed-method design to evaluate the feasibility and impact of a pilot hybrid TNP service with new patients with OUDs entering a MAT program.

Participants were >18 years old and new patients enrolling in MAT for OUD. Participants were excluded if they planned to move out of town within six months or were pending incarceration. Participants were identified by triage questions at MAT intake based on frequency of relevant co-occurring conditions indicating those with greatest need. Positively triaged individuals were referred to the TNP service which was conducted by a hybrid approach (i.e., patient presents to the clinic and is evaluated from a separate room using video-teleconferencing technology). We aimed to schedule participants within two-weeks of 30-days from intake to the MAT program. Consented participants completed questionnaires of feasibility and acceptability (e.g., satisfaction, usefulness) after undergoing a screening TNP evaluation and feedback of the results and recommendations. Participants also were invited to undergo a brief qualitative interview to further assess facilitators and barriers.

Of 57 individuals screened positive, 51 were referred, and 14 were reached to offer TNP. Ten (71.4%) agreed to the TNP evaluation and scheduled an appointment, though 50% had the first appointment scheduled within two weeks of 30-days after intake to MAT. Seven (70%) did not keep the first appointment (no show or cancellation) or were rescheduled due to clinic scheduling. Three were reached to reschedule. All three were unable to keep the appointment, but one did reschedule and keep the third appointment. Of the 4 who attended TNP, only 1 (25%) was within two weeks of 30-days after intake. Of those who attended the TNP appointment, 100% completed the protocol, 75% were satisfied with the evaluation overall, 75% found the evaluation useful, and 67% would recommend TNP to others (one participant did not respond to this question).

Neuropsychological assessment may provide valuable information to improve treatment for those with OUDs. This pilot project revealed that individuals with OUDs can tolerate and are satisfied with a screening TNP evaluation and find the evaluation useful. The primary barrier was reaching referred patients. Treatment engagement among those with SUDs is a common challenge. Those with counselors who coordinated with the clinic schedulers were more likely to be reached and scheduled, suggesting support for regular case management. Other lessons learned and potential future steps are discussed.

Executive functions (EF) are a primary mediator of both typical and atypical functioning, influencing the progression of psychopathology due to their role in supporting self-monitoring/regulation and top-down control of cognitive processes. According to recent models, EF impairments may contribute to the functional decline of patients with substance use disorder (SUD), exacerbating secondary affective and social symptoms. Despite these potential implications, the tools now commonly used to outline neurocognitive, and specifically EF, impairments in patients with addiction are not tailored to this clinical population, having been developed to assess cognitive or dysexecutive deficits in neurology or geriatric patients. Because of their different clinical focus, such tools are frequently unable to fully delineate the dysfunctional EF profile of addiction patients. We here present the development and validation of a novel specific screening battery for executive disorders in addiction: Battery for Executive Functions in Addiction (BFE-A).

151 SUD patients and 55 control persons were recruited for the validation of the BFE-A battery. The battery consists of two computerized neurocognitive tasks (Stroop and Go/No-go tasks) and five digitalized neuropsychological tests (focus: short/long-term memory, working memory, focused attention, verbal/non-verbal cognitive flexibility). The tests are designed to assess executive control, inhibition mechanisms, and attention bias toward drugs of abuse.

In tests of verbal memory, focused attention, and cognitive flexibility, as well as in computerized tasks, inferential statistical analyses revealed lower performance in SUD patients compared to control participants, indicating a lack of inhibitory processes and dysfunctional management of cognitive resources. The investigation of Cohen’s d values has revealed that inhibitory control, verbal/nonverbal fluency, and short/long-term memory are the areas with the most significant impairments.

While the evaluation of EF dysfunctions associated to addiction is a currently underrepresented component of the diagnostic procedure in drug assistance/treatment programs, is also is an essential step for both profiling of patients and design of rehabilitation protocols. Clinical interviews should be complemented by early assessment of cognitive weaknesses and preserved EF skills in order to establishing personalized therapy strategy and perhaps organizing a concurrent phase of cognitive rehabilitation.

Since seminal work by Sherrington, the term interoception refers to the ability to sense modifications of internal bodily states as opposed to the ability to sense stimuli coming from outside the body itself. Despite conceptual changes regarding the afferent signals subserving this type of inner perception, the core of this definition is still valid and widely accepted. The critical contribution of internal state perception to self-regulation as well as higher-order cognitive processes has led to the development of psychometric and observational measures trying to capture individual interoceptive skills, focusing especially on the ability to orient attention to internal sensations. Nonetheless, despite growing interest in interoceptive attention (IAtt), little is known about neurofunctional correlates of our ability to redirect attention to internal sensations and consciously process them, as well as on potential objective biomarkers of IAtt performance.

This study included 36 volunteers who were asked to complete a heart-beat counting task (HCT), a common IAtt task. During both resting-state and HCT, central electrophysiological (EEG, 32 electrodes) and cardiovascular activity (ECG, I lead) were recorded. eLORETA was used to estimate both task-related and resting-state intracortical sources of EEG signals. Statistical non-parametric mapping (SnPM) was used to draw and investigate contrast statistical maps between rest- and task-related cortical current density.

Contrast analyses comparing HCT and resting revealed higher Alpha frequency current density estimates during the task, with primary cortical seed in the right parahippocampal gyrus. Regression analyses of the relationship between IAtt scores and task-related changes in intracortical current density during HCT revealed a positive relationship for the Beta frequency bands with primary cortical seeds in the cingulate gyrus and insula.

Findings add to available literature by further specifying the electrophysiological signature of interoceptive attentiveness, and suggest specific electrophysiological markers as objective measures of individual IAtt skills.

Neuronal dysfunction of the locus coeruleus (LC), the primary producer of norepinephrine, has been identified as a biomarker of early Alzheimer's disease (AD) pathophysiology. Norepinephrine has been implicated in attentional control, and its reduced cortical circulation in AD may be associated with selective attentional difficulties. Additionally, greater pupil dilation indicates greater effort needed to perform a cognitive task, and greater compensatory effort to perform the digit span task has been found in individuals at risk for AD. In this study, we examined associations between a neuroimaging biomarker of the LC and pupil dilation during the Stroop task as a sensitive measure of attentional control.

64 older adults without dementia were recruited from the San Diego community (mean [SD] age = 74.3 [6.3]; 39 cognitively unimpaired and 25 with mild cognitive impairment). All participants underwent magnetic resonance imaging of the LC and generated behavioral data from a computerized Stroop task that included 36 incongruent trials (e.g., GREEN presented in red ink), 36 congruent trials (e.g., GREEN presented in green ink), and 32 neutral trials (e.g., LEGAL presented in green ink) in a randomized presentation. Mean pupil dilation for each trial (change relative to baseline at the start of each trial) was measured at 30 Hz using the Tobii X2-30 system (Tobii, Stockholm, Sweden) and averaged within each Stroop condition. Paired t-tests assessed for differences in mean pupil dilation across incongruent and congruent Stroop conditions. Iterative re-weighted least squares regression was used to assess the association between a rostral LC contrast ratio measure derived from manually marked ROIs and mean pupil dilation during incongruent trials divided by congruent trials, adjusting for age, sex, and education. Follow-up analyses also assessed the association of these variables with mean reaction time (RT) for incongruent trials divided by congruent trials.

Mean pupil dilation significantly differed across conditions (t = 3.74, mean difference = .13, 95% CI [.06, .20]) such that dilation was higher during the incongruent condition (mean [SD] dilation = .18 [.38] mm) relative to the congruent condition (mean [SD] dilation = .05 [.35] mm). A significant association was observed between pupil dilation and LC contrast ratio, such that increased levels of mean dilation during incongruent trials relative to congruent trials were observed at lower levels of LC contrast ratio (i.e., lower LC integrity; r = -.37, 95% CI [-.55, -.13]). This association was not observed for mean dilation during only congruent trials (r = -.08, 95% CI [-.31, .18]). Additionally, neither LC contrast ratio [r = .24, 95% CI [-.02, .46]) nor mean incongruent/congruent pupil dilation (r = .14, 95% CI [-.13, .37]) were associated with incongruent/congruent RT.

Findings suggest that increased pupil dilation during a demanding attentional task is indicative of increased compensatory effort needed to achieve the same level of performance for individuals with reduced LC biomarker integrity. Pupillometry assessment offers a low-cost, non-invasive, and scalable biomarker of LC dysfunction that may be indicative of preclinical AD.

Delayed speech and language development is one of the main diagnostic criteria for autism spectrum disorders (ASD) and is found almost in all children with ASD. Language development in children with ASD may differ from the norm both quantitatively (delayed speech development, reduced vocabulary, scarcity of speech and limitation in its use) and qualitatively (echolalias, violation of speech grammatical structure, difficulties in the communicative use of speech). Studying different aspects of language development in ASD is very important as it provides opportunities for finer diagnostics, as well as for targeted correction of communication disorders.

The study included 34 primary-school-aged children, who were diagnosed ASD using ADOS-2, diagnostic groups included “autism” (24 children) and “autism spectrum” (8 children). Speech development was assessed using the “Korablik” test on 9 parameters: distinguishing sounds; understanding and generating nouns, verbs and syntax; text understanding; sentences repetition. Kaufman test battery (KABC-II) and the Wechsler test (WISC-III) were used to assess non-verbal intelligence. The sample was divided into two subgroups according to an educational program recommended by PMPC (Psychological, Medical and Pedagogical Commission). Group 1 included 15 children, attending program 8.1, which is recommended for children with ASD who reach developmental milestones before starting study. Group 2 included 19 children attending program 8.2, which is recommended for children with ASD who do not reach developmental milestones before starting study.

In general, all children were the best successful in understanding and generating nouns, understanding verbs, and the least successful in understanding text and searching for sound in the word. Comparing subgroups using Mann-Whitney test revealed significant differences in all measured speech parameters, except for word repetition and noun generation. Group 2 demonstrated uneven results for separate subtests - minimum scores in some subtests coexisted with maximum in others. The group also showed uneven scores distribution inside the subtests, for example, half of the children did not cope with the task to determine a sound in a word, while the rest successfully completed at least 83% of the task. A significant positive correlation between all speech subtests was found in the group. Correlation analysis for parameters of speech development, severity of autistic manifestations and non-verbal intelligence revealed a significant direct relationship between the total scores of impressive and expressive speech and IQ and an inverse relationship with the severity of autistic manifestations and disorders of social and communicative behavior. No relationships like described above were found for group 1.

Obtained results indicate variability of reasons for delayed development of various language aspects in children with ASD.

An individual with dementia suffers from cognitive decline affecting not only memory but at least one of the other domains, such as personality, praxis, abstract thought, language, executive functioning, attention, and social skills. Further, the severity of the decline must be significant enough to interfere with daily functions. It is currently unknown whether any of the causes of dementia can be cured. Many challenges confront patients and their families, including a lack of knowledge about dementia and associated treatments; therefore, it is essential to study illness perception regarding dementia-related symptoms in order to improve psychoeducation and lower barriers to seeking assistance. How individuals perceive and make sense of early dementia symptoms can significantly impact their help-seeking behaviors (HS). Exploring illness-perception regarding dementia-related symptoms may contribute to the development of strategies for increasing HS, early diagnosis, and intervention. The objective of this study is to describe aspects of illness perception in cognitively healthy older adults and examine potential correlations with demographic variables, including age, gender, and education.

The cohort comprised 55 cognitively healthy older adults enrolled in a study examining Subjective Cognitive Decline. All participants performed > -1.5 SD on clinical neuropsychological testing. Participants were 70% female and 30% male; and self-identified as White = 78%, Black = 16%, Asian = 2%, Other = 4% and Non-Hispanic = 98%. Participants read a short vignette describing a person experiencing significant memory issues representative of an individual with mild dementia and answered seven follow-up questions regarding the cause of memory problems, the likely course of memory problems, and potential treatments for memory problems. Chi-square analyses examined the endorsement of items in relation to age, gender, and education.

When asked about the likely cause of memory problems, 65% of participants endorsed neurologic disease, 53% of participants endorsed normal aging, 26% endorsed stress, 25% endorsed genes, 4% endorsed fate/luck, and 16% endorsed "Don't know" for likely cause of symptoms. 64% of participants responded "will get worse", 18% "will go up and down", 16% "Don't know", and 2% "Other" in response to the progression of memory problems over time. For "Can he do anything to help [memory problems]?", only 2% responded "No" while 76% responded "Yes" and 22% endorsed "Don't know". On a follow-up question regarding ways an individual could improve his cognitive difficulties, 78% "Social Engagement", 73% "Exercise", 64% endorsed "Medication", 48% "Diet", 42% Psychological Treatment", 29% "Rehabilitation", 9%" Don't know" and 15% "Other." Lastly, 58% of participants reported "Independence", 33% "Identity," 4% "Friends," 4% "Respect," and 1% "Don't know" for things he may risk losing due to memory problems. Age, gender, and education were not associated with any of the above responses (p > .05).

Older adults demonstrate a range of ideas about the cause, course, and potential treatment for memory disorders. Understanding how and what factors impact illness perception is a pivotal step in improving illness perception and ultimately narrowing the gap in health disparities and HS. Further work in a large demographically representative sample is needed on illness perception and how socioeconomic factors, ethnicity, and other mediators interact with its impact on HS for dementia-related symptoms.